The objective of this investigation is to define better methods of quantitating cardiac rejection, reduce myocardial injury during the period of cardiac transplanatation, and prevent rejection crises for better survival of a hemodynamic stable cardiac graft. Previous studies have identified reduction of cardiac output and coronary flow as early hemodynamic consequences of the rejection crisis. These have been correlated with histologic studies regarding degree of rejection and physiologic performance. The ability to quantitate a circulating anti- heart antibody is being investigated and further research research in this area is requested. The so-called anti-heart antibody cross - reacts with antigen from streptococcal membranes. This cross-reactivity with streptococcal membrane antigen allows some degree of quantitation of circulating anti-heart antibody which will react against this membrane. Our current studies suggest that the least amount of endothelium damage which occurs at the time of transplantation, the least likely early rejection is to occur and the antibody response is less. Studies directed towards quantitation of the antibody using the streptococcal membrane antigen, inducing tolerance by repetitious antigen injection using the streptococcal membrane as antigen of both low and high doses, and early immunoparalysis in newborns using membrane antigen by attempting to alter the immune memory system are proposed. With a cross-reactive antigen as described, the possibility of selective destruction or alteration of leukocytic cells may be possible which would allow prolonged survival of a cardiac allograft.